Journal: Psychopharmacology

Article Title: Specificity of a rodent alpha(α)6 nicotinic acetylcholine receptor subunit antibody

doi: 10.1007/s00213-019-05413-x

Figure Lengend Snippet: Evaluation of an alpha(α)6 nicotinic acetylcholine receptor subunit antibody. A western blot of α6 nAChR subunit expression and antigen block in bilateral ventral tegmental tissue punches collected from male Sprague Dawley rats. n=2 animals total. GAPDH is used as a loading control.

Article Snippet: Although, a control antigen (Alomone) blocks the α6 nAChR subunit antibody from binding in the PC12 pheochromocytoma cells, a more standard form of validation is necessary ( Uhlen et al. 2016 ).

Techniques: Western Blot, Expressing, Blocking Assay

Journal: Psychopharmacology

Article Title: Specificity of a rodent alpha(α)6 nicotinic acetylcholine receptor subunit antibody

doi: 10.1007/s00213-019-05413-x

Figure Lengend Snippet: Genetic validation of an alpha(α)6 nicotinic acetylcholine receptor subunit antibody. A.) Western blot and B.) relative band intensity quantification of α6 nAChR subunit expression and antigen block from whole brain tissue collected from male and female WT and α6 KO C57BL/6J mice, n=4 animals/genotype; **p< 0.01 and ***p< 0.001 α6 antibody vs. α6 antibody + antigen normalized signal. GAPDH is used as a loading control.

Article Snippet: Although, a control antigen (Alomone) blocks the α6 nAChR subunit antibody from binding in the PC12 pheochromocytoma cells, a more standard form of validation is necessary ( Uhlen et al. 2016 ).

Techniques: Western Blot, Expressing, Blocking Assay

Journal: Carcinogenesis

Article Title: Activation of the mTOR pathway by low levels of xenoestrogens in breast epithelial cells from high-risk women

doi: 10.1093/carcin/bgr196

Figure Lengend Snippet: RPFNA-derived HRBEC cultures display characteristic non-malignant epithelial phenotypes. ( A ) Micrographs of cell clusters present in independent representative RPFNA samples. ( B ) Early passage pure epithelial cultures derived from clusters similar to those shown in A (Brightfield, × 4 objective). ( C ) Three-dimensional growth pattern of colonies derived from early passage HRBEC cultures in Matrigel. Basal immunolocalization of alpha-6 integrin (blue) and acinar orientation of nuclei (red) in 10 day-old colonies. ( D ) Relative ERα and ERβ protein levels in breast cancer cell lines (T47D, SKBR3 and MCF7), spontaneously immortalized HRBEC lines (IMM-PA024, IMM-PA025 and IMM-PA115) and early passage HRBECs (PA134, PA135, PA136, PA138, PA139 and PA140) quantitated by western blotting. Numerical values of each protein band representing ERα or ERβ obtained by densitometric scanning were normalized to actin levels in the lysate and plotted. Note low to moderate ERα levels in HRBECs relative to T47D and MCF7, but higher than the SKBR3 cell line, HRBECs display a distinctive ER profile unlike conventional ER-positive or ER-negative breast cancer cell lines.

Article Snippet: Colonies fixed with 1:1 methanol:acetone were incubated with anti-alpha-6 integrin (BD Pharmingen, San Diego, CA) followed by fluorescence-tagged secondary antibody and propidium iodide (PI) nuclear counterstain.

Techniques: Derivative Assay, Western Blot

Journal: Chinese Medical Journal

Article Title: Role of p300 in the pathogenesis of Henoch-Schonlein purpura nephritis and as a new target of glucocorticoid therapy in mice

doi: 10.1097/CM9.0000000000000380

Figure Lengend Snippet: Expression of glucocorticoid receptor and resistance gene at mRNA and protein level in each group. (A) Expression of GRα and β, transforming growth factor-β1 and activator protein-1 mRNA in each group. (B, C) Expression of GRα and β, transforming growth factor-β1 and activator protein-1 protein in each group. Glucocorticoid receptor (GR) α expression was significantly higher in Group VI in comparison with Group III ( ∗ P < 0.05); the expression of GRβ did not differ significantly. Meanwhile, p300 knockdown caused a significant increase in the expression of transforming growth factor-β1 and activator protein-1 at the levels of mRNA and protein, which suggests that p300 is involved in the occurrence of glucocorticoid resistance ( ∗ P < 0.05). Group II: Non-knockout model group; Group III: Non-knockout dexamethasone therapy group; Group VI: p300 knockout dexamethasone therapy group.

Article Snippet: The primary antibodies used in this study were as follows: GRα (BOSTER Bio Inc, Wuhan, China), GRβ (Bioss Bio Inc, Beijing, China), TGF-β1 (BOSTER Bio Inc), activator protein (AP)-1 (Bioss Bio Inc), and GAPDH (Santa Cruz Bio Inc, Santa Cruz, USA).

Techniques: Expressing, Comparison, Knockdown, Knock-Out